Jumla DLSO reported the death of the periodic total 31 adult mules With symptoms as abnormal behavior, aggression, changing habits, misalignment proprioception, abnormal pupillary response to light, agalactia, anorexia , ataxia, blindness, circling, colic, coma, cyanosis, reduced stool volume, stool away, constipation, decreased bowel sounds, decreased, absent thirst, hypodipsia, adipsia, dehydration, chewing difficulties or prehending food, disoriented, blunt, dysmetria, dysphagia, dyspnea , salivation, agitation, weakness, press head, shaking his head, head, face, ears, weak jaws static, head, face, ears, chin, nose, nasal discharge, swelling, head, face, neck, tongue hypoesthesia, Hemoglobinuria or myoglobinuria , hyperesthesia, jaundice, unable to stand, increased respiratory rate, mydriasis, move opisthotonus, paraparesis, petechiae or ecchymosis, drive, red or brown urine, reluctantly, seizure or syncope, Skin edema, sudden death, sweating, tetra paresis, tongue weakness , trembling, tremor.
Death within 10-15 minutes after collapsing on the field. These herds were treated with antibiotics and vaccinated against anthrax during this period, the mortality is not checked. On field investigation, obtaining a full history and complete physical examination was found that the horses torn and moldy corn were fed.
Review of Literature:
Penicillium grain mold is probably the second most common grain mold pathogens. It can be caused and P. chrysogenum by different species of Penicillium, including P. oxalicum. Penicillium species are well adapted to survival in many types of bearings. Kernel infection can occur in the field or in storage. Symptoms range from external to internal mold discoloration ("Blue Eye") of the embryo. Symptoms caused by Penicillium found with those of Aspergillus glaucus caused confusion. Most fungi produce mycotoxins, a class of chemical compounds called secondary metabolites. These compounds have a broad spectrum of biological activities, including toxicity of antibiotics (antibacterial and antifungal), acute and chronic (plants, animals and humans), and growth hormone and the regulation (plants and animals). It is not more than one type of mold pathogen of cereals to be rarely present in a storage bin and many grain mold pathogens can be active at the same ambient conditions, the more chance a mycotoxin have produced a large number of contaminated grains. The nature of the toxic effects of mycotoxins is very different. Some mycotoxins acute (ie immediate effect) where a particular organ (liver, kidney) loses complete or partial function; other mycotoxins cause chronic poisoning (ie long term) cause symptoms such as weight loss and reproductive disorders. Still other mycotoxins impair the immune system predisposing the affected animal to a variety of infections or other diseases. For some mycotoxins damage is not permanent and affected animals recover from the ingestion of contaminated food, if you get from food. (Jim Stack,).
Equine leukoencephalomalacia commonly called "Moldy corn poisoning," is a disease of the central nervous system, the horses, mules and donkeys concerns. It is commonly associated with feeding moldy corn over several days to several weeks. The clinical symptoms of the neurological form of equine leukoencephalomalacia connected with horses, apathy, drowsiness, pharyngeal paralysis, blindness, district, support problems, staggering, hyper excitability, seizures and possible lying down. But in some cases, sudden death may be the only clinical signs observed. Once the animals show neurological symptoms, death usually occurs within 48-72 hours. If an animal survives the acute syndrome, neurological deficits were observed. A horse is once again a "dummy" because of its loss of intelligence means. Histologically there may be diffuse vacuolization of hepatocytes, fatty degeneration, centrilobular necrosis with inflammatory cells, bile duct proliferation, bile stasis, increased mitotic figures in hepatocytes, or periportal fibrosis. leukoencephalomalacia disease is usually a fatal neurological disorder with rapid progression of the horses (and other equids) caused by ingestion of fumonisin. Horses with these signs are usually recumbent and comatose in 1-10 days and can tonic-clonic convulsions before dying. In some cases, press frantic behavior such as head, you may experience anxiety, agitation hyper, sweating, and delirium. It is characterized by liquefaction necrosis of the white matter. Liver damage can occur. The extent of the contamination of raw corn with fumonisins varies with geographic location, cultivation and storage, and susceptibility to fungal plant invasion in all phases of growth, storage and processing. The level of fumonisins in raw corn is also influenced by environmental factors such as temperature, humidity and rainfall during preharvest and harvest periods. Fumonisins are associated with high followed by hot, dry weather with periods of high humidity. High fumonisins may also occur in raw corn that has been damaged by insects. Horses, along with rabbits, are species especially vulnerable to the toxic effects of fumonisins. Ruminants, mink and poultry are more resistant than horses, rabbits, catfish and swine to fumonisin. Clinical signs can be 1 to 21 weeks after food intake occur with fumonisin, but usually occur within 2-9 weeks. The time of occurrence depends on the concentration of fumonisins in animal feed. Clinical signs of fumonisin poisoning in horses are usually associated with liquefaction necrosis of the white matter of the brain and progressive ataxia, depression, anorexia, delirium, hiking, recumbency, coma and death. Death can occur from 12 hours – 1 week after onset of clinical symptoms. At autopsy, lesions in the cerebral cortex can be from zero to multifocal areas of hemorrhage and necrosis, the presence of cavitation go liquefaction necrosis. Histologically, multifocal liquefaction necroses in the cerebral cortex with infiltration of macrophages. The differential diagnosis should rabies, equine encephalomyelitis, equine herpes virus, botulism, head injury, and bacterial hepatoencephalopathy meningoencephalitis (Dr. Steve Hooser, Dr. Duane Murphy 2003).
Material and methods:
Mule population in Jumla
A total of 900 mules are a total of 50 members for internal transport of carriers in good mountain district Mule company. Mules were mostly fed with whole corn. These grains are usually from the market only a small part of it is bought used in domestic production. These grains have mold upto15-20% and not processed before feeding.
Preliminary investigations on the ground
The autopsy revealed severe congestion of death Mule of the liver, lungs, Speen, heart, liquid serosangqinus in pleural cavity.Haemorrhage in the gastric mucosa. Preliminary cause of sudden death was suspected for moldy grain poisoning.
Collection of blood for bacteriological culture of smear
The liver, lung, spleen, heart tissue for histological examination
Blood for bacteriological, parasitological investigation
The liver, lung, spleen, heart, intestine for toxicological analysis
Faecal samples for endoparasite examination.
Serum for serological examination
Food crops: maize, in grief for the identification of the fungal culture, limit of Mules in herds with toxin binder, adaptogen, immunomodulater, vitaminBcomplex provided treatment and preventive measure.
Bacteriological culture of tissue samples, blood, swab: not reveal bacterial growth. Blood parasite toxin in tissue-negative. Chemical: negative. Intestinal parasites: Mixed Strongyels spp.
Penicillium, Aspergillus, Candida spp on mycological media.
110 * 6 * 10 to 10 CFU / g Penicillium colonies recorded in food samples.
Histopathological changes: Liver: fatty degeneration of the cell infiltration as nodules hepatocytes.Mononuclear few
Lungs: Perivascular inflammation. The infiltration of mononuclear cells in the nodules.
Kidney: Deep medullary region shows infiltration of mononuclear cells .
Spleen: The number of white blood cells appear in the white pulp can be increased. Suggestive of chronic viral disease.
Serum sample: turn out positive for J/E
Treatment and control measures recommended:
Suggestions for proper drying of grain before feeding
Two per cent copper sulfate in the grain is mixed prior to feeding. toxin binders commercial Varishta, Toxicurb @ 1kg/tone grain for 15 days with liver tonic, Immunomodulaters, vitamin B complex.
Result and discussion:
Approximately 15-20% moldy corn with Penicillium spp regularly these deaths, but significant, abrupt, herd. Intermitent during post rainy season fed infestated beat to death by toxin. Histopathological changes in the tissues of the lungs, liver, kidneys fungus are similar to the results other workers. Histologically, a center of necrosis is observed with no apparent structure. The transition between normal and necrotic tissue often show hemorrhage, edema, congested blood vessels and neuronophagia. In animals with the hepatotoxic syndrome, livers will be swollen and a diffuse yellow-brown color. Irregular nodules and pale foci can be seen in the liver parenchyma. (Dr. Steve Hooser, Dr. Duane Murphy 2003). Pathogenicity of Fusarium has shown that hepatic congestion with mild Triaditis, lung congestion and spleen lymphoid hyperplasia (Karki 2003) causes. In addition, more of a positive response to treatment with toxin binder, adaptogen, immunomdulater confirms the sudden death was moldy corn poisoning. Enhanced monitoring of the completion of this investigation is proposed.
The results of this study indicates that moldy feed grains and ingredients are infested appears to toxic mushroom as a health hazard for new animals and poultry.Simultonious toxin binder, adaptogen, such as liver tonic, mineralmixture drugs and promises Immunomodulaters contribute to health risks for livestock and poultry production are taken into account .
1: moldy CORN POISONING HORSES (LeukoencephalomalaciaMark Equine Russell, PhD, Don Department of Animal Sciences Scott, Ph.D., Department of Botany and Plant Pathology William Hope, DVM, Department of Veterinary Clinical Lafayette Extension science cooperative university west ServicePurdue, IN 47 907, n TÉCNICO Boletim 15 -. http://www.micotoxinas.com.br/ access 06.21.2007
2: definitive diagnosis Moldy Corn Poisoning (Equine leukoencephalomalacia, Fumonisin Toxicity) in Horses: Dr. Steve Hooser, ADDL Toxicologist Dr. Duane Murphy, ADDL Pathologist Spring 2003 Newsletter http://www.addl.purdue.edu/newsletters/2003/spring/finaldx.shtml. Retrieved 6/21/2007
3: to prevent the harmful effects of mycotoxins Feed effects on the health of your horse and performance.Mycotoxins in Equine: By Trevor K. Smith, PhD, Pag www.ecmagazine.net/…/mycotoxin2.jpg access 21/06/2007
4: Moulds and mycotoxins in maize grain: Jim Stack, Extension plant pathologist Research Division of the Institute for Agriculture and Natural Resources at the University of Nebraska-Lincoln working with the counties and the U.S. Department of Agriculture.http: / / CBC. homestead.com / archives.html, accessed 21/06/2007
5: Toxocurb: www.polchemgroup.com .
6: Varishta: www.varshagroup.com.
7: Evaluation of Fusarium graminearum pathogenicity in mice. Kedar B. Karki: PP14, Vetcon 2003, 7 National Veterinary Conference 2003, Nepal Veterinary Association